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Query: UMLS:C0038454 (stroke)
 147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The first generation of an integrated, totally implantable electrohydraulic total artificial heart was designed for long-term cardiac replacement. The system consists of an elliptical blood pump with an interatrial shunt, Medtronic-Hall 27 mm and 25 mm inflow and outflow valves, respectively, an energy converter consisting of an axial-flow, hydraulic pump driven by a brushless DC motor, and an electronics system with transcutaneous energy transmission and telemetry. Energy is supplied by internal nickel-cadmium rechargeable batteries that supply power for 20 min and external silver-zinc batteries that are designed to supply energy to run the system for 5 hr. The blood pump consists of a single layer diaphragm cast from Biolon, with joined right and left ventricles sharing a common base. The dynamic stroke volume is 84 ml, and maximum cardiac output is 9.2 L/min at a heart rate of 110 beats/min on the mock circulation. A 4.3 mm diameter interatrial shunt is used to balance the volumetrically coupled ventricles. The energy converter pumps hydraulic fluid alternately between ventricles, with controlled, active filling in one ventricle during the systolic phase of the other ventricle. Internal or external controllers adjust the heart rate and motor speed to maintain normal atrial filling pressures and full stroke. Electromagnetic induction is used to transfer energy through the skin and a bidirectional infrared data link incorporated within the transcutaneous energy transmission coils is used to transmit information. The entire system is being assembled and refined for long-term animal implant studies.
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PMID:Development of a totally implantable artificial heart. 145 55

Health problems at a heavy metal mining Superfund site were surveyed using prevalence information from 1980-85. Current environmental exposures include lead and cadmium in drinking water, mine wastes, and surface soils. Age- and sex-specific illness rates in whites in an exposed town (Galena) were compared with similar rates in two control towns. Multivariate analyses of morbidity data examined statistically significant risk factors for relevant illness in the three towns. Mortality rates for 1980-85 for white residents of Galena and for the U.S. were compared using univariate analysis. Among residents of the three towns who had lived there at least 5 years prior to 1980, there was either a statistically significant or borderline excess reported prevalence in Galena of chronic kidney disease (females aged greater than or equal to 65), heart disease (females aged greater than or equal to 45), skin cancer (males aged 45-64), and anemia (females aged 45-64). Multivariate analyses revealed statistically significant associations of stroke, chronic kidney disease, hypertension, heart disease, skin cancer, and anemia with variables related to Galena exposure. Personal physicians were contacted to confirm the information provided by the subjects; validity was good for all reported illnesses except chronic kidney disease. A statistically significant excess of deaths from hypertensive disease (females aged greater than or equal to 65), ischemic heart disease (males and females aged greater than or equal to 65), and stroke (females aged greater than or equal to 65) was found in residents of Galena City. This study confirms that environmental agents in Galena are associated with, and may have contributed to, the causation of several chronic diseases in residents of this community. Further studies are recommended.
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PMID:Health problems in Galena, Kansas: a heavy metal mining Superfund site. 236 37

The purpose of this study was to evaluate the time course of cardiac function during recovery from upright bicycle exercise in patients with coronary artery disease. Twelve patients with coronary artery disease performed a symptom-limited exercise test on a cycle ergometer. Left ventricular function was continuously monitored during exercise and recovery with a computerized cadmium telluride detector following the intravenous injection of technetium-labeled red blood cells. Although the end-diastolic volume (153.4 +/- 76.1 ml) and end-systolic volume (100.5 +/- 67.3 ml) at the end of exercise were significantly higher than the respective resting values, stroke volume (52.8 +/- 16.1 ml) and ejection fraction (38.0 +/- 12.2%) were not different from the respective resting values. The recovery of cardiac output was relatively slow compared with that of heart rate, because stroke volume rose sharply early in recovery. The rise in stroke volume was chiefly a result of a significant decrease in end-systolic volume between 1 and 4 minutes of recovery. These changes may result from an immediate afterload reduction coupled with a relatively slow decrease in sympathetic stimulation. The time course of cardiac function during recovery from exercise in cardiac patients is substantially different from that of normal subjects and may be a sensitive way to evaluate the peripheral vascular function and deteriorated cardiac function in cardiac patients.
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PMID:Beat-to-beat evaluation of cardiac function during recovery from upright bicycle exercise in patients with coronary artery disease. 238 9

We investigated changes in the pulmonary carbon monoxide diffusing capacity (DLco) during the cold pressor test (CPT) on 25 normal subjects. In 10 of them we also observed changes in circulatory parameters by a computerized dual cadmium telluride detector system, using an equilibrium radionuclide blood-pool label. DLco and DLco per unit of alveolar volume (DLco/VA) averaged in the control period were 29.4 +/- 4.1 ml/min/mm Hg, 6.1 +/- 0.8 ml/min/mm Hg/l (mean +/- SD). During the 2nd minute of CPT, DLco increased by 3.6 +/- 1.5% and DLco/VA by 5.1 +/- 1.5% (mean +/- SE). The systemic blood pressure increased by 17% (mean increase) whereas the heart rate and the stroke volume remained unchanged. The increases were small but significant (p less than 0.05, p less than 0.01, respectively). We conclude that the increase in DLco is due to cold-induced systemic vasoconstriction followed by a passive shift of blood into the pulmonary vasculature.
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PMID:Effect of cold pressor test on carbon monoxide diffusing capacity in normal subjects. 260 71

The degree of exercise-induced cardiac dysfunction and its relation to the anaerobic threshold were evaluated in 23 patients with chronic heart disease. A symptom-limited exercise test was performed with a cycle ergometer with work rate increased by 1 W every 6 seconds. Left ventricular function, as reflected by ejection fraction, was continuously monitored with a computerized cadmium telluride detector after the intravenous injection of technetium-labeled red blood cells. The anaerobic threshold (mean, 727 +/- 166 ml/min) was determined by the noninvasive measurement of respiratory gas exchange. As work rate rose, the left ventricular ejection fraction increased but reached a peak value at the anaerobic threshold and then fell below resting levels. Ejection fraction at rest, anaerobic threshold, and peak exercise were 41.4 +/- 11.3%, 46.5 +/- 12.0%, and 37.2 +/- 11.0%, respectively. Stroke volume also increased from rest (54.6 +/- 17.0 ml/beat) to the point of the anaerobic threshold (65.0 +/- 21.2 ml/beat) and then decreased at peak exercise (52.4 +/- 18.7 ml/beat). The slope of the plot of cardiac output versus work rate decreased above the anaerobic threshold. The anaerobic threshold occurred at the work rate above which left ventricular function decreased during exercise. Accurate determination of the anaerobic threshold provides an objective, noninvasive measure of the oxygen uptake above which exercise-induced deterioration in left ventricular function occurs in patients with chronic heart disease.
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PMID:Detecting abnormalities in left ventricular function during exercise by respiratory measurement. 268 75

In developed countries, hypertension represents one of the most frequent diseases and is one of the most important risk factors of arteriosclerotic vascular disease e.g. to myocardial infarction or cerebral apoplexy. The etiology of hypertension is unknown in about 90% of cases. The heavy metals cadmium and lead occur in increasing amounts in the human environment. Numerous epidemiological studies and investigations using experimental animals have dealt with the putative relationship between cadmium and lead, and hypertension. The results to date have been quite controversial; thus the issue appears to be unresolved at present. In the present study scalp hair samples were collected from 100 non-smoking 30-to-50-year-old men. After washing, the samples were digested with a mixture of nitric and sulfuric acid in a teflon bomb and analyzed by flameless atomic absorption spectroscopy. For 90% of the test persons the cadmium hair values were in the range of 0 to 1400 micrograms/kg; the corresponding range for hair lead was 0 to 13,000 micrograms/kg. Correlation with diastolic or systolic blood pressure was neither found for cadmium or lead. The test persons with the highest cadmium or lead load were not hypertensive. Some factors should be considered when comparing the present results with those of other investigators reporting a positive correlation in the question under consideration. 1. Previous studies in man frequently did not sufficiently take smoking habits into account. This is essential, however, because, in addition to cadmium and lead, nicotine and carbon monoxide are also constituents of tobacco smoke and contribute to an increase in blood pressure. 2. Previous investigations generally employed blood samples, which is disadvantageous in comparison with the analysis of hair because blood samples do not reflect long-term exposition, which is important in the etiology of chronic diseases. Correlation between hypertension and levels of long-term cadmium and lead exposure in man seem to be unlikely in light of the present results. Nevertheless, numerous potential effects should be considered to obtain further insight in the complex pathogenesis of hypertension.
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PMID:[Correlation of blood pressure and cadmium and lead content of the hair in nonsmoking males]. 275 43

Male rabbits received 20 micrograms/ml of cadmium in drinking water for nine months. At the end of the treatment aortic vascular resistance was increased, whereas maximum rate of increase in left ventricular pressure, aortic blood flow, stroke volume, cardiac output, left ventricular minute work, and left ventricular stroke work were reduced. Arterial blood pressure, heart rate, and the index of myocardial oxygen consumption were not modified. The exposed rabbits also showed reduced pressor responses to vagotomy, increased cardiovascular responses to angiotensin I and II and isoprenaline, and lower responses to serotonin and guanethidine; the bradycardia induced by clonidine was augmented; the cardiovascular effects of bilateral carotid occlusion, hexamethonium, phenylephrine, histamine, acetylcholine, tyramine, papaverine and verapamil were unaltered. In the treated rabbits cadmium was appreciably higher in the kidney than in the heart; however, renal concentrations of cadmium were lower than those reported as critical for workers exposed to cadmium. Zinc was increased in the kidney but not in the heart, whereas copper remained unchanged in the examined organs. In rabbits treated with cadmium the increased aortic vascular resistance and the reduced myocardial contractility contribute to preserve a haemodynamic equilibrium without alteration of blood pressure and heart rate; the question of whether a similar condition may be present in people exposed to cadmium with normal cardiovascular parameters is discussed.
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PMID:Mechanisms of cardiovascular regulation in male rabbits chronically exposed to cadmium. 375 11

Veratridine blocks Na(+)-channel inactivation and causes a persistant Na(+)-influx. Exposure of hippocampal slices to 10 microM veratridine led to a failure of synaptic transmission, repetitive spreading depression (SD)-like depolarizations of increasing duration, loss of Ca(+)-homeostasis, a large reduction of membrane potential, spongious edema and metabolic failure. Normalization of the amplitude of the negative DC shift evoked by high K+ ACSF 80 min after veratridine exposure was taken as the primary endpoint for neuroprotection. Compounds whose mechanisms of action includes Na(+)-channel modulation were neuroprotective (IC50-values in microM): tetrodotoxin 0.017, verapamil 1.18, riluzole 1.95, lamotrigine > or = 10, and diphenylhydantoin 16.1. Both NMDA (MK-801 and PH) and non-NMDA (NBQX) excitatory amino acid antagonists were inactive, as were NOS-synthesis inhibitor (nitro-L-arginine and L-NAME) Ca(2+)-channel blockers (cadmium, nimodipine) and a K(+)-channel blocker (TEA). Lubeluzole significantly delayed in time before the slices became epileptic, postponed the first SD-like depolarization, allowed the slices to better recover their membrane potential after a larger number of SD-like DC depolarizations, preserved Ca2+ and energy homeostasis, and prevented the neurotoxic effects of veratridine (IC50-value 0.54 microM). A concentration of lubeluzole, which was 40 x higher than its IC50-value for neuroprotection against veratridine, had no effect on repetitive Na(+)-dependent action potentials induced by depolarizing current in normal ACSF. The ability of lubeluzole to prevent the pathological consequences of excessive Na(+)-influx, without altering normal Na(+)- channel function may be of benefit in stroke.
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PMID:Altered Na(+)-channel function as an in vitro model of the ischemic penumbra: action of lubeluzole and other neuroprotective drugs. 903 12

1. Electrical events and intracellular calcium concentration ([Ca2+]) imaged using fluo-3 and laser scanning confocal microscopy were simultaneously monitored in single smooth muscle cells freshly isolated from guinea-pig vas deferens or urinary bladder. 2. Images obtained every 8 ms, during stepping from -60 to 0 or +10 mV for 50 ms under voltage clamp, showed that a rise in [Ca2+] could be detected within 20 ms of depolarization in five to twenty small (< 2 micrometer diameter) 'hot spots', over 95 % of which were located within 1.5 micrometer of the cell membrane. Depolarization at 30 s intervals activated hot spots at the same places. 3. Cd2+ or verapamil abolished both hot spots and Ca2+-activated K+ current (IK,Ca). Caffeine almost abolished hot spots and markedly reduced IK,Ca. Cyclopiazonic acid, which raised basal global [Ca2+], decreased the rise in hot spot [Ca2+] and IK,Ca amplitude during depolarization. These results suggest that Ca2+ entry caused Ca2+-induced Ca2+ release (CICR). 4. Under voltage clamp, hot spot [Ca2+] closely paralleled the rise in IK,Ca and reached a peak within 20 ms of the start of depolarization, but the rise in global [Ca2+] over the whole cell area was much slower. Step depolarization to potentials positive to -20 mV caused hot spots to grow in size and coalesce, leading to a rise in global [Ca2+] and contraction. Ca2+ hot spots also occurred during the up-stroke of an evoked action potential under current clamp. 5. It is concluded that the entry of Ca2+ in the early stages of an action potential evokes CICR from discrete subplasmalemma Ca2+ storage sites and generates hot spots that spread to initiate a contraction. The activation of Ca2+-dependent K+ channels in the plasmalemma over hot spots initiates IK,Ca and action potential repolarization.
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PMID:Ca2+ images and K+ current during depolarization in smooth muscle cells of the guinea-pig vas deferens and urinary bladder. 966 Aug 87

Mercury, cadmium, and other heavy metals have a high affinity for sulfhydryl (-SH) groups, inactivating numerous enzymatic reactions, amino acids, and sulfur-containing antioxidants (NAC, ALA, GSH), with subsequent decreased oxidant defense and increased oxidative stress. Both bind to metallothionein and substitute for zinc, copper, and other trace metals reducing the effectiveness of metalloenzymes. Mercury induces mitochondrial dysfunction with reduction in ATP, depletion of glutathione, and increased lipid peroxidation; increased oxidative stress is common. Selenium antagonizes mercury toxicity. The overall vascular effects of mercury include oxidative stress, inflammation, thrombosis, vascular smooth muscle dysfunction, endothelial dysfunction, dyslipidemia, immune dysfunction, and mitochondrial dysfunction. The clinical consequences of mercury toxicity include hypertension, CHD, MI, increased carotid IMT and obstruction, CVA, generalized atherosclerosis, and renal dysfunction with proteinuria. Pathological, biochemical, and functional medicine correlations are significant and logical. Mercury diminishes the protective effect of fish and omega-3 fatty acids. Mercury, cadmium, and other heavy metals inactivate COMT, which increases serum and urinary epinephrine, norepinephrine, and dopamine. This effect will increase blood pressure and may be a clinical clue to heavy metal toxicity. Cadmium concentrates in the kidney, particularly inducing proteinuria and renal dysfunction; it is associated with hypertension, but less so with CHD. Renal cadmium reduces CYP4A11 and PPARs, which may be related to hypertension, sodium retention, glucose intolerance, dyslipidemia, and zinc deficiency. Dietary calcium may mitigate some of the toxicity of cadmium. Heavy metal toxicity, especially mercury and cadmium, should be evaluated in any patient with hypertension, CHD, or other vascular disease. Specific testing for acute and chronic toxicity and total body burden using hair, toenail, urine, serum, etc. with baseline and provoked evaluation should be done.
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PMID:The role of mercury and cadmium heavy metals in vascular disease, hypertension, coronary heart disease, and myocardial infarction. 1740 90


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